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Arch Ophthalmol. 2001;119:1212-1213.

The presence of blood or blood debris in the anterior chamber can increase intraocular pressure (IOP). Vitreous hemorrhage can also lead to secondary glaucoma, producing a "ghost cell glaucoma" (GCG).^1-2 Ghost cells (GCs) are degenerated spherical erythrocytes that partially lose their hemoglobin content by aging for a long period in the vitreous. Changes begin after a few days and are usually completed within 3 weeks. Hemoglobin abandons the red blood cell and forms clumps that adhere to vitreous bands. Hemoglobin that remains in the red blood cell becomes denatured and binds to the internal surface of the cell membrane, forming granules (Heinz bodies).³ Once formed, GCs may remain intact for months, moving freely within the vitreous. Neither fresh erythrocytes nor GCs are able to pass through an intact anterior hyaloid membrane; thus, a hyaloid injury must be present for these cells to be found in the anterior segment.^2-3 Since GCs are rigid, they have difficulty passing through the trabecular meshwork. They tend to accumulate in its middle and external portions, whereas fresh erythrocytes pass 3 times more easily to the external portion and from there to the Schlemm canal.^{1, 3}

Increased IOP usually occurs about 2 to 4 weeks after the injury, but it may also take from 1 week to many months to develop.^2-3 It is a complication that often requires surgical intervention with profuse and repeated lavage of the anterior chamber or vitrectomy to remove the hemorrhagic tissue.^2-4

We describe a patient who developed vitreous hemorrhage and GCG after a snake bite. There was no evidence of anatomic alteration of the anterior hyaloids.

Report of a Case
A 44-year-old male farmer was seen in the emergency department of our institution (Hospital San Juan de Dios, National University of Colombia, Bogotá) 72 hours after sustaining a snake bite (Bothrops athrox) in his right foot. The patient was admitted to the hospital and treated for respiratory distress syndrome and hemorrhagic syndrome with renal and cerebral involvement. Two days later, after recovery from respiratory distress and renal failure, he complained of bilateral visual loss.

On examination, his visual acuity was hand motions in the right eye and light perception in the left eye. The left eye showed inferior and temporal subconjunctival hemorrhage (Figure 1), stromal and epithelial corneal edema, ++++ cells and flare in the anterior chamber, and dense anterior vitreous hemorrhage (Figure 2). The IOP was 17 mm Hg OD and 40 mm Hg OS. Dilated indirect ophthalmoscopy showed a dense vitreous hemorrhage in both eyes. Results of B-scan ultrasonography confirmed bilateral vitreous hemorrhage with incomplete posterior vitreous detachment.

View larger version (33K): [in this window] [in a new window] Figure 1. Left inferior subconjunctival hemorrhage as part of hemorrhagic syndrome.

View larger version (22K): [in this window] [in a new window] Figure 2. Left slitlamp photograph showing corneal edema and elevated number of ghost cells in anterior chamber.

With an initial diagnosis of GCG in the left eye, a paracentesis and aqueous sampling were performed in the left eye. Cytologic examination of the aqueous humor disclosed the presence of GCs. Meanwhile, the IOP in the right eye rose to 28 mm Hg, and treatment was begun with 0.4% apraclonidine hydrochloride twice daily, 0.4% timolol maleate twice daily, and a prostaglandin derivative 3 times daily in both eyes. A diagnostic paracentesis in the right eye confirmed the presence of GCs.

Results of B-scan ultrasonography performed 2 weeks later showed little or no resolution of the vitreous hemorrhage. Both eyes were treated with standard 3-port posterior vitrectomy. Cytologic examination of the vitreous showed the presence of GCs (Figure 3). Bilateral indirect ophthalmoscopy showed optic nerve pallor with a cup-disc ratio of 0.2 and attenuated retinal vascular tree and fovea reflex loss. The IOP normalized in the right eye and visual acuity improved to 20/70. The IOP normalized in the left eye, but the visual acuity was counting fingers at 40 cm because of a rhegmatogenous retinal detachment with macular involvement.

View larger version (25K): [in this window] [in a new window] Figure 3. Spherical erythrocytes with vacuoles and partial loss of hemoglobin (ghost cells) in vitreous (Papanicolaou, original magnification x100).

Comment
Bilateral GCG secondary to snake poisoning has not yet been described in the literature, based on our MEDLINE search of the medical literature since the initial description of GCG in 1976 to the present.

Ghost cell glaucoma has been associated with diabetic vitreous hemorrhage in a phakic eye without previous trauma or surgery as well as in other rare cases.^5-6 Snake venoms, especially those from crotalids, as in the case of Bothrops, contain proteolytic enzymes capable of breaking tissue proteins, thereby acting as hemorrhagic factors. Thrombinogenic and thrombinoid enzymes with fibrinolytic action have also been detected. Viper's venom alters vascular resistance and, often, vascular integrity. It produces changes in blood cells and coagulation mechanisms as well as alterations in central nervous system, cardiovascular, and pulmonary dynamics.⁷ Hyaluronidase is also present in all American viperous poisons studied to date.⁸ Hyaluronidase, collagenase, and other proteolytic enzymes present in the Bothrops venom may decrease the vitreous viscosity and alter the anterior hyaloid permeability. This physiologic disruption may allow migration of the GCs in the aqueous, causing the secondary glaucoma affecting both eyes.

Ghost cells were identified by cytologic examination of vitreous and aqueous humor, centrifuged and stained with Papanicolaou stain⁹ (Figure 1). Sometimes, the vitreous has "hemolytic cells" that are actually macrophages with hemosiderin and erythrocyte fragments.

Ophthalmologists should be aware that snake bite can cause visual loss. Early diagnosis and prompt treatment to reduce the number of blood cells and GCs may increase the potential for recovery.

AUTHOR INFORMATION

Ledy Rojas, MD; Gabriel Ortiz, MD; Myrian Gutiérrez, MD; Sonia Corredor, MD
Bogotá, Colombia

Corresponding author: Ledy Rojas, MD, Departamento de Oftalmología, Hospital San Juan de Dios, Carrera 10 Calle 1, Bogotá, Colombia (e-mail: ledy_rojas{at}yahoo.com).

REFERENCES
1. Campbell DG, Simmons RJ, Grant WM. Ghost cells as a cause of glaucoma. Am J Ophthalmol. 1976;81:441-440. PUBMED 2. Montenegro MH, Simmons RJ. Ghost cell glaucoma. Int Ophthalmol. 1994;34:111-114. 3. Campbell D, Schertzer RM. Ghost cell glaucoma. In: Ritch R, Shields MB, Krupin T, eds. The Glaucomas. St Louis, Mo: CV Mosby Co; 1996:1277-1284. 4. Campbell DG, Essigmann EM. Hemolytic ghost cell glaucoma: further studies. Arch Ophthalmol. 1979;97:2141-2146. ABSTRACT 5. Mansour AM, Chess J, Starita R. Nontraumatic ghost cell glaucoma: a case report. Ophthalmic Surg. 1986;17:34-36. PUBMED 6. Rodriguez FJ, Foos RY, Lewis H. Age-related macular degeneration and ghost cell glaucoma. Arch Ophthalmol. 1991;109:1305-1305. 7. Russell FE, Dart RC. Toxic effects of animal toxins. In: Amdur MO, Doul J, Klaassen CD, eds. Casarett and Doull's Toxicology: The Basic Science of Poison. 4th ed. New York, NY: Pergamon Press; 1991:743-803. 8. Bolaños R. Serpientes, Venenos y Ofidismo en Centroamérica. San Jose, Costa Rica: Editorial Universidad de Costa Rica; 1984:48-49. 9. Rosenthal DL, Mandell DB, Glasgow BJ. Eye. In: Bibbo M, ed. Comprehensive Cytopathology. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1997:493-509.

SECTION EDITOR: W. RICHARD GREEN, MD